Oral three-times-daily bupropion IR was effective and generally well tolerated in the treatment of major depressive disorder (MDD). It was as efficacious and as well tolerated as some tricyclic antidepressants (TCAs) and the selective serotonin reuptake inhibitor (SSRI) fluoxetine. Moreover, it was associated with less somnolence and weight gain than some TCAs. Twice-daily bupropion SR was also efficacious and generally well tolerated in the treatment of MDD. It was as effective as and had a generally similar tolerability profile to some SSRIs, but had the advantage of less somnolence and sexual dysfunction. The efficacy of bupropion XR in terms of primary efficacy measures was established in two of six well designed placebo-controlled studies. Bupropion XR also demonstrated efficacy in terms of some secondary outcomes in five of these studies. Additionally, bupropion XR was similar, in terms of the primary efficacy outcomes, to the SSRI escitalopram in two placebo-controlled trials and to the serotonin-norepinephrine reuptake inhibitor (SNRI) venlafaxine extended release (XR) in two trials (one of which was placebo-controlled), but not in a third placebo-controlled trial where venlafaxine XR was better than bupropion XR. It was generally as well tolerated as escitalopram and venlafaxine XR, but was associated with less sexual dysfunction than escitalopram. Available clinical data suggest that bupropion is an effective and generally well tolerated option in the treatment of MDD, with the newer formulations having the advantage of reduced frequency of daily administration.

Pharmacological properties of bupropion

As with all antidepressants, the precise mechanism of action of bupropion in MDD is unknown, although bupropion selectively inhibits dopamine and norepinephrine reuptake. The reuptake inhibition potential of bupropion is greater for dopamine than for norepinephrine. Importantly, bupropion does not affect serotonergic pathways and does not act on postsynaptic histamine, alpha- or beta-adrenergic, dopamine or acetylcholine receptors.

Time to reach maximum plasma concentration (Cmax) varied between bupropion formulations (IR ~ 2 h, SR ~ 3 h and XR ~ 5 h). A decreased number of peak plasma levels were associated with bupropion SR and XR, compared with bupropion IR. However, bioequivalent systemic exposure (as assessed by Cmax and area under the plasma concentration-time curve) was established between all formulations of bupropion and its three pharmacologically active metabolites. Steady state is reached within 8 days. Bupropion is extensively metabolized, mainly by cytochrome P450 (CYP) isoenzymes or via carbonyl reduction. As the active metabolites of bupropion reach higher steady-state concentrations than those of bupropion, these metabolites may be of clinical importance. Bupropion has an elimination half-life (t 1/2) of 20–21 hours and is predominantly (87%) excreted in the urine as metabolites. The t 1/2 of the active metabolites of bupropion are ~20, ~33 and ~37 hours. There is potential for drug-drug interactions between bupropion and drugs that affect CYP2B6 and 2D6 metabolism, drugs that are substrates of these isoenzymes and drugs that affect metabolism in general.

Therapeutic efficacy of bupropion

Three-times-daily bupropion IR was effective in the treatment of MDD in a 6-week randomized, double-blind clinical trial in adults with moderate to severe disease, demonstrating greater improvement from baseline in several efficacy measures relative to placebo. Moreover, bupropion IR was as effective as the SSRI fluoxetine, the TCAs nortriptyline, amitriptyline and doxepin, and the atypical antidepressant trazodone in reducing symptoms of depression and anxiety assessed by several efficacy measures in 6- to 13-week trials in adults with MDD.

Similarly, twice-daily bupropion SR was effective in the treatment of MDD in 8-week, randomized, double-blind clinical trials in adults with moderate to severe disease, demonstrating greater improvements from baseline in several efficacy measures relative to placebo. In addition, bupropion SR was effective in preventing relapse in one 52-week relapse-prevention study in a similar patient population. In comparative trials, there were no significant differences between bupropion SR and the SSRIs sertraline or fluoxetine in adults and the SSRI paroxetine in elderly patients with moderate to severe disease in randomized studies of 6- to 16-weeks’ duration. Furthermore, bupropion SR was as effective as the SSRI sertraline and the SNRI venlafaxine XR with respect to remission rates (primary efficacy measure) in patients who were switched from citalopram therapy because of a lack of remission of symptoms or because they could not tolerate citalopram in the large, randomized, multicentre STAR*D trial. In the same study, bupropion SR was shown to be as effective as the serotonin receptor agonist buspirone, in terms of remission rates, when used to augment citalopram therapy in a similar patient population. There were some benefits with bupropion SR relative to buspirone therapy as demonstrated by a greater reduction from baseline in self-rated 16-item Quick Inventory of Depressive Symptomology (QIDS-SR-16) score and a lower QIDS-SR-16 score with bupropion compared with buspirone therapy at study end.

Two of six placebo-controlled trials in adult and elderly patients with moderate to severe MDD demonstrated greater improvements from baseline in the 30-item self-rated Inventory of Depressive Symptomology scale or Montgomery-Asberg Depression Rating Scale (MADRS) total scores (primary efficacy measures) with once-daily bupropion XR relative to placebo. However, in the trial involving elderly patients, although significant reduction from baseline in MADRS total scores in bupropion XR relative to placebo recipients in the last-observation-carried-forward (LOCF) analysis (primary efficacy measure) was not observed, significant improvements from baseline were observed in the protocol-defined observed-case or per-protocol analyses and according to the rank analysis of covariance and robust regression analysis. Benefit with respect to some secondary measures was observed with bupropion XR relative to placebo in five of six placebo-controlled efficacy studies in adults and the elderly.

There were no significant differences between bupropion XR and the SSRI escitalopram in terms of the change from baseline in the 17-item Hamilton Rating Scale for Depression (HAM-D-17) total score (primary efficacy measure) in patients with moderate to severe disease in placebo-controlled studies of 8 weeks’ duration. Similarly, in two 8- and 12-week studies, one of which was placebo-controlled, in patients with similar disease, there were no significant differences between bupropion XR and the SNRI venlafaxine in terms of primary (MADRS total score) or secondary (HAM-D-17 total score) efficacy measures. Additionally, in the 12-week study, more patients achieved remission with bupropion XR than venlafaxine XR therapy. However, in one 8-week placebo-controlled study, venlafaxine XR was better than bupropion XR in terms of MADRS total scores (primary efficacy measure).

Tolerability of bupropion

All three formulations of bupropion (IR, SR or XR) were generally well tolerated in patients with moderate to severe MDD. Adverse event-related withdrawal rates in pooled analyses were 5–11% in bupropion IR, SR or XR recipients. Overall, the most common treatment-emergent adverse events reported in bupropion IR, SR or XR versus placebo recipients were headache (20–26% vs 20–23%), dry mouth (16–28% vs 7–18%) and nausea (13–23% vs 8–19%); agitation was another common treatment-emergent adverse event reported in 32% of bupropion IR compared with 22% of placebo recipients. Bupropion SR and XR were also well tolerated in terms of their effects on sexual functioning in patients with MDD.

Most adverse events associated with bupropion SR or XR relative to placebo were mild to moderate in severity. However, there is a dose-dependent risk of seizures (0.4% with bupropion IR 300–450 mg/day; 0.1% with bupropion SR 100–300 mg/day, increasing to 0.4% with bupropion SR 400 mg/day; and 0.1% with bupropion XR ?450 mg/day) associated with the use of bupropion. Although the effect of bupropion (IR, SR or XR) on suicidality is not clear, it is recommen ded that patients should be monitored closely. In general, the effects of bupropion (IR, SR or XR) on vital signs (systolic and diastolic blood pressure and heart rate) were small, although some changes (largely an increase in ?12% of patients) in these parameters with bupropion XR were of potential concern or were sustained (in 3–11% of patients) during therapy.

Although the tolerability profile of bupropion (IR, SR or XR) was generally similar to that of TCAs (nortriptyline, amitriptyline and doxepin), an atypical antidepressant (trazodone), SSRIs (including sertraline, fluoxetine and escitalopram) and an SNRI (venlafaxine XR) in patients with moderate to severe MDD, some adverse events were reported in fewer bupropion than comparator recipients.

Bupropion SR and XR were associated with less sexual dysfunction than SSRIs, such as sertraline and escitalopram. Bupropion XR had a more favourable effect on sexual function than venlafaxine XR in one study, which assessed the parameter as the primary outcome measure, but not in two others where sexual function was assessed as a secondary outcome measure. Bupropion IR and SR were associated with less somnolence relative to some TCAs and SSRIs. On the other hand, the incidence of dry mouth was higher with bupropion IR and SR than with some SSRIs, but lower than that observed with some TCAs. In patients receiving citalopram therapy augmented with bupropion SR or buspirone in the STAR*D trial, discontinuation rates due to intolerance were lower with bupropion SR plus citalopram than with buspirone plus citalopram.

Although bupropion IR, SR and XR were associated with a weight gain of >2.3 kg (>5 lb), the incidence of weight gain was ~4-fold lower with bupropion IR than with TCAs. Bupropion (IR, SR or XR) was also associated with a weight loss of >2.3 kg (>5 lb). However, the incidence of weight loss with bupropion IR was approximately twice that observed with TCAs. No clinically significant changes in weight were observed in bupropion SR or placebo recipients after 52 weeks of therapy.

Zopiclone is known colloquially as a “Z-drug”. Other Z-drugs include zaleplon (Sonata) and zolpidem (Ambien and AmbienCR) and were initially thought to be less addictive and/or habit-forming than benzodiazepines. However, this appraisal has shifted somewhat in the last few years as cases of addiction and habituation have been presented. It is recommended that zopiclone be taken on an “as needed” basis. Daily or continuous use of the drug is not usually advised. While it acts on the same benzodiazepine receptors as the benzodiazepine family of drugs it is not classed as a benzodiazepine (with which it shares a number of characteristics and effects) due to its differing molecular structure. Zopiclone is classed as a cyclopyrrolone derivative. [Wikipedia.org]

Since 1987 when zopiclone was introduced into clinical practice, extensive evaluations have shown that some rebound changes can be detected in healthy individuals. In patients with insomnia more than 20 studies have assessed rebound. Rebound can be found in such patients, but is usuallymore frequent and present in greater intensity in comparison groups given triazolam.

Studies in the elderly have been carefully reviewed by Soldatos and his colleagues. Some deterioration in the soundness of sleep has been detected but the amount of rebound insomnia following zopiclone discontinuation is relatively weak. Although one would certainly expect rebound in a hypnotic with a half-life of around 5 h, the frequency and severity of such rebound seems definitely less than those observed with comparative benzodiazepines such as triazolam and temazepam.

Longer-term studies have been designed to detect withdrawal as well as rebound phenomena. A large scale study in France recorded any reactions to stopping zopiclone after it had been taken for up to 12 months. Over a thousand patients took part, most of whom stopped abruptly. In only 1.3% of the overall population was there substantial evidence of any withdrawal. The symptoms comprised anxiety, irritability, malaise and perceptual changes, which are characteristic of a sedativetype withdrawal reaction. Two parallel studies evaluated the withdrawal following long-term zopiclone (somnosan, ximovan) and long-term zolpidem. Thirty eight percent of those who withdrew from zopiclone had apparent symptoms, but these were also found in 27% of those who continued. Most of the withdrawal symptoms related to sleep complaints. Excluding these, no treatment-emergent increase in withdrawal symptoms was found.

An evaluation has beenmade of the utility of zopiclone substitution in facilitating the withdrawal of flunitrazepam. Twenty-four volunteers with insomnia and a history of long-termbenzodiazepine hypnotic usewere assessedwith both subjective and objective measures during a 5-week substitution with zopiclone and subsequent withdrawal or continuation on flunitrazepam. Withdrawal from flunitrazepam was accompanied aworsening of sleep quality, both subjectively and objectively. No such deterioration was seen in the zopiclone - substituted groups.

Lemoine and Ohayon completed a much larger scale study. Over 1000 patients being treated with a hypnotic were allocated to one of three treatments: gradual substitutionwith zopiclone; immediate substitutionwith zopiclone (somnosan, ximovan); remained on their benzodiazepine. The gradual and abrupt substitution group had improved sleep during this initial phase; the abrupt substitution group did best. During withdrawal, the last group (benzodiazepine-using) fared worst and more resumed their medication. The PSG withdrawal effects of zopiclone (7.5 mg), zolpidem (10 mg) and triazolam (0.25 mg) as compared with placebo were studied in 38 healthy subjects over 4 weeks. Slight, non-significant rebound effects on sleep continuity were detected after withdrawal of zopiclone and zolpidem. Total sleep time and sleep efficiency were lower the first night after cessation of triazolam.

A very detailed review of zopiclone noted its proven efficacy and good tolerability.With respect to withdrawal, clinical trials showed no evidence for significant rebound insomnia. The risk of withdrawal reactions was very low, although dependency and abuse have been reported.

Post-marketing surveillance and pharmacovigilance data contain few convincing cases of withdrawal from zopiclone. Most consist of rebound insomnia, but there are a few instances of withdrawal convulsions following high-dose dependence. A reviewof 25 zopiclone discontinuation studies found rebound effects andwithdrawal symptoms to be minimal.

via www.anxietyonlinepharmacy.com

Thanks to the “Prozac (fluoxetine) revolution” of the 1980s and 1990s, a majority of people in America know someone who has used antidepressants. Over 34 million people in the United States have been issued prescriptions for Prozac (fluoxetine) or another selective serotonin reuptake inhibitor (SSRI). In other words, one American in ten has used

antidepressants and studies have estimated that one in six people will have a major depressive episode in their lives (Figure 1.2).

The term “depressive” does not just signify a simple feeling of sadness, but can also refer to any mental disorder with symptoms of moodiness and melancholy — anxiety or eating disorders, for example. Depression is no longer a disease that is shameful or that must be kept hidden. Depression is also no longer as debilitating as it was in the early twentieth century, before the development of antidepressant drugs. Still, the costs of depression to society in terms of lost work, treatment, and other associated expenses have been estimated to be in excess of $30 billion per year. Even with all the progress in antidepressant research, there is an even bigger push to find more antidepressants that work faster and better since rates of depression appear to be growing every year.

But how can a chemical change a person’s outlook on life? If the root of depression is caused by a problem in a person’s life, is it right to take a pill rather than confront the problem? Or is depression something organic, a brain imbalance that can only be cured by taking antidepressants? Are antidepressants, in essence, changing a person’s personality? Furthermore, how well do they work (all hype aside)?

Antidepressants became a media obsession in the early 1990s largely following the publication of Prozac Nation, Elizabeth Wurtzel’s memoir of adolescent depression and its unexpected “cure” by a new kind of antidepressant called fluoxetine, better known as Prozac. Listening to Prozac (fluoxetine), psychiatrist Peter Kramer’s best-selling book, continued the drug’s run of publicity with its descriptions

of formerly depressed patients becoming social, focused, and successful professionals. But on the trail of Listening to Prozac’s success are many other books, which protest that Prozac (fluoxetine) and other antidepressants from the same family (selective serotonin reuptake inhibitors) do not deserve the reputation that the media has given them. Furthermore, other researchers have published findings that refute the effectiveness of selective serotonin reuptake inhibitors (SSRIs) as compared to older antidepressants, straight talk therapy, or even herbal mood-boosters such as St. John’s wort. One study even claims that SSRIs are no better than placebo (the sugar pill used as a control in clinical studies) and might, in fact, be making patients worse.

via: www.anxietyonlinepharmacy.com

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Definition of Alprazolam (Xanax, Xanor, Tafil)

Alprazolam is a tranquilizer. It belongs to a group of drugs called benzodiazepines. In the United States alprazolam is sold under brand name Xanax.

Purpose of Alprazolam (Xanax, Xanor, Tafil)

The United States Food and Drug Administration has approved alprazolam to treat anxiety, panic disorder, and anxiety associated with depression. Occasionally alprazolam is used to treat alcohol withdrawal, but it is not FDA-approved for this use, and is not normally the first drug tried in treating alcohol withdrawal symptoms.

Description of Alprazolam (Xanax, Xanor, Tafil)

Alprazolam is classified as a benzodiazepine. Benzodiazepines are sedative-hypnotic drugs that help to relieve nervousness, tension, and other anxiety symptoms by slowing the central nervous system. To do this, they block the effects of a specific chemical involved in the transmission of nerve impulses in the brain, decreasing the excitement level of the nerve cells.

All benzodiazepines cause sedation, including drowsiness and reduced mental alertness. However, one benefit of alprazolam is that it causes somewhat less drowsiness than many other benzodiazepine drugs.

Alprazolam comes in 0.25-mg, 0.5-mg, 1-mg and 2-mg tablets, and 1-mg/ml solution.

KEY TERMS

Benzodiazepines—A group of central nervous system depressants used to relieve anxiety or to induce sleep.

Glaucoma—A group of eye diseases characterized by increased pressure within the eye significant enough to damage eye tissue and structures. If untreated, glaucoma results in blindness.

Recommended dosage of Alprazolam (Xanax, Xanor, Tafil)

The recommended initial adult dose for anxiety is 0.25–0.5 milligrams (mg) taken three times daily. This dosage may be increased every three to four days to a maximum total of 4 mg daily. Dosage for alcohol withdrawal usually totals from 2–2.5 mg daily given in several small doses throughout the day.

The starting dose for treating panic disorder is 0.5 mg three times daily. This dosage may be increased every three to four days until the total daily dosage ranges from 2–10 mg. The total amount should be divided in at least three even daily doses. Average doses for anxiety associated with depression range from 2.5–3 mg daily divided into even doses.

Precautions of Alprazolam (Xanax, Xanor, Tafil)

Alprazolam should not be used by patients who are pregnant, have narrow angle glaucoma, take ketoconazole or itraconazole, or those who are allergic to this or any other benzodiazepine drug. The dose of alprazolam must be carefully regulated and individualized in the elderly (over age 60), people with liver or kidney disease, and those taking other medications used to treat mental disorders.

Because alprazolam is a nervous system and respiratory depressant, it should not be taken with other similar depressants, such as alcohol, other sedatives, sleeping pills, or tranquilizers. People taking this drug should not drive, operate dangerous machinery, or engage in hazardous activities that require mental alertness at least until they see how the drug affects them.

Alprazolam should be used under close physician supervision in patients with history of substance abuse. Like other benzodiazepines, alprazolam can be habit-forming. Risk and severity of dependence appears greater in patients taking doses larger than 4 mg daily. However, smaller doses may cause dependence if alprazolam is taken longer than 12 weeks.

Suddenly discontinuing alprazolam after several weeks may cause uncomfortable symptoms of withdrawal. Withdrawal symptoms in people who have taken alprazolam three months or longer may include seizures, anxiety, nervousness, and headache. Patients should discuss with their doctor how to gradually discontinue alprazolam use to avoid such symptoms.

Side effects of Alprazolam (Xanax, Xanor, Tafil)

The most common side effects of alprazolam include sedation, dizziness, drowsiness, insomnia, and nervousness. The intensity of these side effects usually declines gradually and subsides in about eight weeks. A drop in blood pressure and an increase in heart rate may also occur in people who are taking alprazolam.

Decreased sex drive, menstrual disorders, and both weight gain and weight loss has been associated with alprazolam use. People who experience the side effects of stomach upset, nausea, vomiting, and dry mouth should eat frequent, small meals and/or chew sugarless gum. Alprazolam has been associated with both diarrhea and constipation, as well as tremor, muscle cramps, vision disturbances, and rash.

Interactions of Alprazolam (Xanax, Xanor, Tafil)

Alprazolam interacts with a long list of other medications. Anyone starting this drug should review the other medications they are taking with their physician and pharmacist for possible interactions. The most severe interactions occur with antifungal medications, such as ketoconazole, itraconazole, and fluconazole. These are associated with alprazolam toxicity (excessive sedation, fatigue, slurred speech, slowed reactions and other types of psychomotor impairment).

Estrogens (female hormones), erythromycin (an antibiotic), fluoxetine (Prozac, Sarafem), cimetidine (Tagamet), isoniazid, and disulfiram (Antabuse) can increase the effects of alprazolam. Carbamazepine can make alprazolam less effective. When alprazolam is combined with other sedative drugs (tranquilizers, sleeping pills) or alcohol, its depressants effects are more intense. These combinations should be avoided.

Resources

1. Kay, Jerald. Psychiatry: Behavioral Science and Clinical Essentials. Philadelphia: W. B. Saunders Company, 2000.
2. Lacy, Charles F. Drug Information Handbook. Hudson, OH: Lexi-Comp, Inc. 2002.
3. Pharmacia and Upjohn Company Staff. Product Information: Xanax, alprazolam. Kalamazoo, MI: Pharmacia and Upjohn Company, 1999. Ajna Hamidovic, Pharm.D.

Insomnia is one of the most common complaints seen in medicine. Incidence and prevalence estimates vary slightly depending on the methodology, but commonly cited figures are that approximately one-third of Americans have symptoms of acute or intermittent insomnia, and that approximately 10% have chronic insomnia. Over the past several decades, there have been great strides in understanding the pathophysiology of insomnia as well as documenting the efficacy of pharmacologic and nonpharmacologic treatments. There are now sufficient data to allow for meta-analyses to be conducted in insomnia, which help compare effect sizes across studies. This chapter provides an overview of the development of insomnia, information required to make a diagnosis of insomnia, the various recognized insomnia diagnoses, and the pharmacologic, cognitive, and behavioral treatments available.

Modern, prescription hypnotic medications are typically those that act as benzodiazepine receptor agonists (also called BZRAs). The classic benzodiazepine hypnotics include flurazepam (Dalmane, Dalmadorm) (long half-life), temazepam (Restoril) (moderate half-life), and triazolam (Halcion) (short half-life). Due to extreme next-day sedation from an active metabolite with an extremely long half-life, flurazepam is rarely recommended for the routine treatment of insomnia. Triazolam is rarely prescribed today, after several well-publicized instances of anterograde amnesia associated with its use (though at a higher dose that is no longer recommended). Newer, non-benzodiazepine BZRAs include the short-half-life medications zolpidem (Ambien, Stilnox) and zaleplon, and the moderate-half-life medications eszopiclone and zolpidem extended release. Relatively new in the arsenal of insomnia treatments is the melatonin receptor agonist ramelteon. This medication has the sole distinction of being the only prescription hypnotic that is not a scheduled drug in the USA, due to data that found no abuse potential or next-day impairment in test subjects. Melatonin is also available in over-the-counter (OTC) form, but this is typically not a first-line treatment recommendation, given the lower production standards for purity and accuracy of dose per pill required of dietary supplements.

In prescribing hypnotics for insomnia, it is helpful to match the type of sleep complaint with the half-life of the medication. For example, a person presenting only with difficulty initiating sleep at the beginning of the night will do well with a short-half-life medication, and have less risk of next-day sedation. Sleep maintenance complaints are typically matched with a moderate-half-life medication, in order to provide sedation further into the sleep episode. Individuals with either type of insomnia paired with significant daytime anxiety may do well with a single, longer-half-life medication that can address both complaints. This is where the anxiolytic medication clonazepam is often used in insomnia treatment.

There is also no consensus in the field of sleep medicine as to whether hypnotics should be used on a nightly or a PRN basis by insomniacs. What is more agreed upon is that hypnotic medications tend  not to be used well by individuals with a history of abuse of medication or substances, as they may escalate doses without approval or even against medical advice. The newer hypnotic medications possess much lower risk of respiratory suppression in an overdose scenario, and hence they are safer for people with psychiatric conditions than were the older, barbiturate medications.

As a general rule, the field of sleep medicine is in favor of the short-term use of hypnotic medication for insomnia, in the range of a few nights to three weeks. This is where the consensus ends. Many sleep specialists are uncomfortable prescribing hypnotics for insomnia over the long term, due to concerns about the potential for dependence and tolerance. Most hypnotics do not have data to address the concern of possible loss of efficacy over extended use, although a recent study of  eszopiclone showed stable efficacy through a 6-month double-blind study and an additional 6-month open-label, extension period. In contrast, other sleep specialists recognize that some individuals come to clinical attention with fixed beliefs that only a hypnotic medication will work for them, and are not open to alternative treatments. Others may accept only short-term hypnotic use or refuse this route altogether, opting instead for nonpharmacologic treatments.

Curiously, hypnotics are not the sleep aids most commonly prescribed by physicians, but rather the antidepressant trazodone. It is perhaps the case that physicians are more comfortable prescribing low doses of sedating antidepressant medications to treat insomnia, though there is a paucity of efficacy data in this area for people who are not depressed but just have insomnia. Insomniacs themselves will commonly opt for OTC sleep aids, which typically contain antihistamines, diphenhydramine, or doxylamine succinate. Alcohol is also frequently used as self-medication for insomnia. While certainly able to help someone fall asleep, alcohol will significantly disrupt sleep later in the night due to rebound CNS activation, it is a potent REM suppressant, and its diuretic properties can also disrupt sleep due to bathroom visits.